The first two authors contributed equally to this work.
Chronic Augmentation of the Parasympathetic Tone to the Atrioventricular Node: A Nonthoracotomy Neurostimulation Technique for Ventricular Rate Control During Atrial Fibrillation
Article first published online: 5 OCT 2009
© 2010 Wiley Periodicals, Inc.
Journal of Cardiovascular Electrophysiology
Volume 21, Issue 2, pages 193–199, February 2010
How to Cite
MISCHKE, K., ZARSE, M., SCHMID, M., GEMEIN, C., HATAM, N., SPILLNER, J., DOHMEN, G., RANA, O., SAYGILI, E., KNACKSTEDT, C., WEIS, J., PAUZA, D., BIANCHI, S. and SCHAUERTE, P. (2010), Chronic Augmentation of the Parasympathetic Tone to the Atrioventricular Node: A Nonthoracotomy Neurostimulation Technique for Ventricular Rate Control During Atrial Fibrillation. Journal of Cardiovascular Electrophysiology, 21: 193–199. doi: 10.1111/j.1540-8167.2009.01613.x
This study was supported by grants from the German Atrial Fibrillation competence NETwork (AFNET) and by Biotronik GmbH&Co. KG, Berlin, Germany.
Dr. Schauerte reports serving as a consultant to Biotronik. He received compensation for participation in a speaker's bureau relevant to this topic. No other conflicts of interest were declared.
- Issue published online: 26 JAN 2010
- Article first published online: 5 OCT 2009
- Manuscript received 5 June 2009; Revised manuscript received 19 July 2009; Accepted for publication 5 August 2009.
- atrial fibrillation;
- vagus nerve;
- atrioventricular node;
- cardiac neurostimulation;
- rate control
Long-Term Cardiac Neurostimulation.Introduction: The right inferior ganglionated plexus (RIGP) selectively innervates the atrioventricular node. Temporary electrical stimulation of this plexus reduces the ventricular rate during atrial fibrillation (AF). We sought to assess the feasibility of chronic parasympathetic stimulation for ventricular rate control during AF with a nonthoracotomy intracardiac neurostimulation approach.
Methods and Results: In 9 mongrel dogs, the small endocardial area inside the right atrium, which overlies the RIGP, was identified by 20 Hz stimulation over a guiding catheter with integrated electrodes. Once identified, an active-fixation lead was implanted. The lead was connected to a subcutaneous neurostimulator. An additional dual-chamber pacemaker was implanted for AF induction by rapid atrial pacing and ventricular rate monitoring. Continuous neurostimulation was delivered for 1–2 years to decrease the ventricular rate during AF to a range of 100–140 bpm. Implantation of a neurostimulation lead was achieved within 37 ± 12 min. The latency of the negative dromotropic response after on/offset or modulation of neurostimulation was <1 s. Continuous neurostimulation was effective and well tolerated during a 1–2 year follow-up with a stimulation voltage <5 V. The neurostimulation effect displayed a chronaxie-rheobase behavior (chronaxie time of 0.07 ± 0.02 ms for a 50% decrease of the ventricular rate during AF).
Conclusion: Chronic parasympathetic stimulation can be achieved via a cardiac neurostimulator. The approach is safe, effective, and well tolerated in the long term. The atrioventricular nodal selectivity and the opportunity to adjust the negative dromotropic effect within seconds may represent an advantage over pharmacological rate control. (J Cardiovasc Electrophysiol, Vol. 21, pp. 193-199, February 2010)